Copyright
©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Aug 27, 2020; 12(8): 423-435
Published online Aug 27, 2020. doi: 10.4254/wjh.v12.i8.423
Published online Aug 27, 2020. doi: 10.4254/wjh.v12.i8.423
Review: Pathogenesis of cholestatic liver diseases
Raquel T Yokoda, Department of Anatomic and Clinical Pathology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, United States
Eduardo A Rodriguez, Department of Gastroenterology, Hepatology and Nutrition, University of Utah, Salt Lake City, UT 84132, United States
Author contributions: Yokoda RT and Rodriguez EA wrote the paper and approved the final version.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Eduardo A Rodriguez, FACP, MD, Assistant Professor, Department of Gastroenterology, Hepatology and Nutrition, University of Utah, 30 N 1900 E, Room 4R118, Salt Lake City, UT 84132, United States. eduardo.rodriguez@hsc.utah.edu
Received: May 6, 2020
Peer-review started: May 6, 2020
First decision: May 24, 2020
Revised: June 7, 2020
Accepted: August 1, 2020
Article in press: August 1, 2020
Published online: August 27, 2020
Processing time: 110 Days and 10.3 Hours
Peer-review started: May 6, 2020
First decision: May 24, 2020
Revised: June 7, 2020
Accepted: August 1, 2020
Article in press: August 1, 2020
Published online: August 27, 2020
Processing time: 110 Days and 10.3 Hours
Core Tip
Core tip: Several factors can condition bile flow derangements including environmental triggering factors, bile transport obstruction and conditions that alter bile concentration. Sustained pro inflammatory signaling associated with genetic and/or epigenetic dysregulation can condition a chronic dysfunctional state that can lead to a fibrogenic state with loss of homeostasis and sometimes malignant transformation.